Bacterial superantigens induce rapid and T cell receptor V beta-selective down-regulation of L-selectin (gp90Mel-14) in vivo.

Upon challenge of mice with bacterial superantigens such as staphylococcal enterotoxin B, several facets of TCR V beta-selective acute T-cell alterations can be observed, which include acute T cell priming, and systemic lymphokine release followed by ligand-specific unresponsiveness. Prompted by experiments showing that stimulation of T cells by phorbol esters in vitro results in rapid shedding of the L-selectin homing receptor, we investigated the expression of adhesion molecules on superantigen-responsive T cells in vivo. Here we show that bacterial superantigens cause TCR V beta-specific loss of L-selectin. Down-regulation of L-selectin was selective, since the expression of other lymphocyte surface receptors was not changed. L-Selectin down-regulation represents a superantigen-induced immediate cell surface alteration and was not observed on T cells stimulated by TCR-specific antibodies. Loss of expression was almost complete within 30 min, and recovered 50 h after challenge. The results suggest that acute loss of L-selectin is a hallmark of T cell activation by bacterial superantigens that may result in profound changes of T lymphocyte recirculation pathways.